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Its evolution involves a slow progression of insulitis with both inflammation and destruction of β-cells. Moreover, it can be clearly stated that T1D is a T-cell-mediated autoimmune disease. The chapter also looks into the immunologic, genetic, and clinical studies, which provide a comprehensive description of disease pathogenesis and to a lesser extent its etiology. The major discovery of the autoimmune origin of T1D is derived in large part from the availability of two spontaneous animal models of the disease-namely, the non-obese diabetic (NOD) mouse and the Bio-Breeding (BB) rat. This chapter focuses on insulin-dependent diabetes mellitus (IDDM), now called type 1 diabetes (T1D). JEAN-FRANÇOIS BACH, in The Autoimmune Diseases (Fourth Edition), 2006 Publisher Summary Prevention and intervention trials are aiming to halt the beta cell–autoimmune process but the results of these trials have not altered the way in which to treat patients with type 1 diabetes. The progression toward clinical onset is associated with a loss of beta cells, and the disease is predictable through HLA typing and test of IAA, GADA, IA-2A, and ZnT8A. The pathogenesis is likely to be controlled by CD8 + T cells recognizing autoantigen–peptides on HLA class I proteins expressed on the beta cell surface. Individuals with two or more islet autoantibodies will go on to develop type 1 diabetes (100%) but it may take 20 years. Individuals, who have developed IAA, GADA, or both, may develop yet other autoantibodies against IA-2 (IA-2A), ZnT8 transporter (ZnT8A), or both. Environmental factors such as virus may be a triggering factor for IAA and GADA, which appear in a way that is associated with human leukocyte antigen (HLA). Standardized tests for insulin autoantibodies (IAA) or GAD65 (GADA) have made it possible to demonstrate that the disease is triggered often during the first years of life. Several non-HLA genetic factors either contribute to the genetic etiology or to the progression toward the clinical onset of the disease. The disease may be diagnosed at any age but only in individuals who have certain HLA-DR-DQ-susceptibility haplotypes. The classical symptoms are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss.
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The subsequent lack of insulin leads to increased blood and urine glucose. Type 1 diabetes, formerly known as juvenile diabetes or insulin-dependent diabetes, results from the specific autoimmune destruction of the pancreatic islet beta cells. Åke Lernmark, Shehab Alshiekh, in Encyclopedia of Immunobiology, 2016 Abstract Numerous metrics (costs, patient outcomes, etc.) demonstrate that specialists (endocrinologists) provide more effective care for those with T1DM than nonspecialists. Significant advances in terms of disease management, afforded by technological innovations related to insulin analogues and more, set the foundation for marked reductions in hemoglobin A 1c (HbA 1c) and improved diabetes care. There is a growing appreciation that T1DM, rather than being a singular disease, may be a heterogeneous disorder with a common phenotype at clinical presentation/diagnosis. Įxtensive efforts continue to be directed at preventing and reversing the disease, but although there has been progress toward this goal, at present there is no universally accepted means for doing so in a public health care setting.
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The risk for the disease can be ascertained through a combination of immunologic, genetic, and metabolic markers of disease. The long-held model describing the natural history of T1DM has been extensively readdressed, and there is a greater appreciation for the disorder's heterogeneity in pathogenesis and symptomatic presentation. The pancreas of T1DM patients possesses an islet immune infiltrate derived from a variety of immunologic phenotypes, is reduced in size and weight, and is subject to unusual exocrine features. The disorder is clearly polygenic (over 40 loci impacting susceptibility identified to date), yet over half of disease susceptibility for T1DM is provided by the major histocompatibility complex (MHC).
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Throughout the globe, the incidence of T1DM is increasing at 3% to 5% per year. Type 1 diabetes mellitus (T1DM) is a disorder resulting from a chronic autoimmune destruction of the insulin-producing pancreatic beta cells.